Kuster H, Opravil M, Ott P, Schlaepfer E, Fischer M, Günthard H F, Lüthy R, Weber R, Cone R W
Department of Internal Medicine, University Hospital Zurich, Switzerland.
Am J Pathol. 2000 Jun;156(6):1973-86. doi: 10.1016/S0002-9440(10)65070-5.
We report detailed quantitative analysis of human immunodeficiency virus-1 (HIV-1) p24 and HIV-1 RNA in tonsil biopsies from 13 patients with early, asymptomatic HIV infection before and during combination antiretroviral therapy. Using fluorescent microscopy in conjunction with reverse transcriptase-polymerase chain reaction of frozen tissue sections, we show that plasma and tissue viral loads decreased by approximately 3 logs during the 1-year treatment period, with good correlation between the HIV-1 p24 and HIV-1 RNA response in tissue. The decrease of tissue viral load was delayed compared to plasma viral load, possibly explained by the observation that the amount of follicular dendritic cell-associated virus correlated best with the area under the curve of plasma HIV-1 RNA throughout the last 12 weeks. Before and during treatment, the relative proportions of HIV-1 on follicular dendritic cells and within mononuclear cells remained constant, suggesting similar decay characteristics in these two lymphoid tissue compartments. However, viral p24 or RNA remained almost always detectable in tissue despite full suppression of HIV-1 RNA in plasma, and increased even after short-term rebounds in plasma viral load. Thus, full and sustained suppression of viral replication was required to efficiently decrease viral load in lymphoid tissue, but complete abolition of residual viral replication was not achieved.
我们报告了对13例早期无症状HIV感染患者在接受联合抗逆转录病毒治疗之前和期间扁桃体活检组织中人类免疫缺陷病毒1型(HIV-1)p24和HIV-1 RNA的详细定量分析。通过将荧光显微镜与冷冻组织切片的逆转录聚合酶链反应相结合,我们发现,在1年的治疗期内,血浆和组织中的病毒载量下降了约3个对数级,组织中HIV-1 p24与HIV-1 RNA反应之间具有良好的相关性。与血浆病毒载量相比,组织病毒载量的下降有所延迟,这可能是由于观察到在过去12周内,滤泡树突状细胞相关病毒的量与血浆HIV-1 RNA曲线下面积的相关性最佳。在治疗前和治疗期间,HIV-1在滤泡树突状细胞和单核细胞内的相对比例保持不变,这表明这两个淋巴组织区室中的病毒衰减特征相似。然而,尽管血浆中的HIV-1 RNA得到了完全抑制,但组织中的病毒p24或RNA几乎总是可以检测到,甚至在血浆病毒载量短期反弹后还会增加。因此,需要完全且持续地抑制病毒复制才能有效降低淋巴组织中的病毒载量,但并未实现完全消除残留病毒复制。